It is a common practice to maintain soil fertility based on the paddy-upland rotation with green manure in the subtropical region of China. However, rare studies are known about greenhouse gas (GHG) emissions from the paddy-upland rotation with green manure incorporation. Therefore, we conducted a field experiment of two years to compared with the effect of two kinds of green manure (CV: Chinese milk vetch and OR: Oilseed rape), and two kinds of cropping system (DR: double rice system and PR: paddy-upland rotation) on greenhouse gases emissions. We have found that the annual accumulation of CH₄ of Chinese milk vetch-rice-sweet potato || soybean was significantly reduced by 32.95%∼63.22% compared with other treatments, mainly because Chinese milk vetch reduced the abundance of methanogens by reducing soil C/N ratio. Meanwhile increasing soil permeability resulting from paddy-upland rotation also reduced soil CH₄ emission. However, The annual accumulation of N₂O of Chinese milk vetch-rice-sweet potato || soybean was increased by 17.39%∼870.11% compared with other treatments, mainly attributed to paddy-upland rotation decreased soil pH and nosZ abundance and increased nirK and nirS, thus enhancing N₂O emission, meanwhile the Chinese milk vetch incorporation and its interaction with the paddy-upland rotation has greatly enhanced the contents of NO₃⁻-N and abundance of ammonia-oxidizing archaea (AOA). The area-scaled global warming potential (GWP) and the biomass-scaled greenhouse gas emissions intensity (GHGI) of Chinese milk vetch-rice-sweet potato || soybean was reduced by 19.01%∼50.69% and 5.38%∼35.77% respectively. Thereby, the Chinese milk vetch-rice-sweet potato || soybean cropping system was suitable for agricultural sustainable development.

Short-term exposure to air pollution has pro-thrombotic effects and triggers thrombo-embolic events such as myocardial infarction or stroke in adults. This study evaluates the association between short-term variation in air pollution and treatments for acute thrombo-embolic events among the whole Belgian population. In a bidirectional time-stratified case-crossover design, we included 227,861 events treated with endovascular intervention and 74,942 with antithrombotic enzymes that were reimbursed by the Belgian Social Security between January 1st, 2009 and December 31st, 2013. We compared the concentrations of particulate matter (PM) air pollution (PM₁₀ and PM₂.₅), as estimated at the municipality level on the day of the event (lag 0) and two days earlier (lag 1 and lag 2) with those of control days from the same month, matched by temperature and accounting for day of the week (weekend vs week days). We applied conditional logistic regression models to obtain odds ratios (OR) and their 95% CI for an increase of 10 μg/m³ (PM₁₀) or 5 μg/m³ (PM₂.₅) in pollutant concentrations over three lag days (lag 0, 1 and 2). We observed significant associations of PM₁₀ and PM₂.₅ with treatment of acute thrombo-embolic events at the three lags. The strongest associations were observed for air pollution concentrations on the day of the event (lag0). Increases of 10 μg/m³ PM₁₀ and 5 μg/m³ PM₂.₅ on lag0 increased the odds of events treated with endovascular intervention by 2.7% (95%CI:2.3%–3.2%) and 1.3% (95%CI:1%–1.5%), respectively, and they increased the odds of events treated with antithrombotic enzymes by 1.9% (95%CI:1.1–2.7%) and 1.2% (95%CI:0.7%–1.6%), respectively. The associations were generally stronger during autumn months and among children. Our nationwide study confirms that acute exposure to outdoor air pollutants such as PM₁₀ or PM₂.₅ increase the use of medication and interventions to treat thrombo-embolic events.

Inflammation may play an important role in the association between exposure to polycyclic aromatic hydrocarbons (PAHs) and atherosclerotic cardiovascular disease (ASCVD) risk. However, the underlying mechanisms remain unclear.To investigate the association of PAHs exposure with ASCVD risk and effects of mean platelet volume (MPV) or Club cell secretory protein (CC16) on the association.A total of 2022 subjects (689 men and 1333 women) were drawn from the baseline Wuhan residents of the Wuhan-Zhuhai Cohort study. Data on demography and the physical examination were obtained from each participant. Urinary monohydroxy PAH metabolites (OH-PAHs) levels were measured by a gas chromatography-mass spectrometry. We estimated the association between each OH-PAHs and the 10-year ASCVD risk or coronary heart disease (CHD) risk using logistic regression models, and further analyze the mediating effect of MPV or plasma CC16 on the association by using structural equation modeling.The results of multiple logistic regression models showed that some OH-PAHs were positively associated with ASCVD risk but not CHD risk, including 2-hydroxyfluoren (β = 1.761; 95% CI: 1.194–2.597), 9-hydroxyfluoren (β = 1.470; 95% CI: 1.139–1.898), 1-hydroxyphenanthrene (β = 1.480; 95% CI: 1.008–2.175) and ΣOH-PAHs levels (β = 1.699; 95% CI: 1.151–2.507). The analysis of structural equation modeling shows that increased MPV and increased plasma CC16 levels contributed 13.6% and 15.1%, respectively, to the association between PAHs exposure and the 10-year ASCVD risk (p < 0.05).Exposure to PAHs may increase the risk of atherosclerosis, which was partially mediated by MPV or CC16.

Cadmium (Cd) exposure is recognized as an important risk factor for psychological health, but suitable physical activity may relieve depression. However, it remains unknown whether physical activity (PA) can reduce the effect of cadmium exposure on depression. Therefore, a cross-sectional data from National Health and Nutrition Examination Survey (NHANES) 2015–2018 was used. The Nine-item Patient Health Questionnaire (PHQ-9) was used to assess depression among the participants. PA was calculated according to the metabolic equivalent (MET), weekly frequency, and duration of each activity. Logistic regression and restricted cubic spline models were used to examine the associations of Cd and depression. A total of 5560 adults aged 20 years and above were finally included in this study. The results indicated a positive correlation between blood Cd and depression. The multivariate-adjusted ORs (95% CI) of the highest quartile were 2.290 (1.754–2.990) for depression, which was still significant after controlling other heavy metals (P < 0.05). Under Cd exposure, the high intensity of physical activity group had the lowest risk of depression (OR = 2.226, 95%CI: 1.447–3.425), while the group with no physical activity had the highest risk (OR = 2.443, 95%CI: 1.382–4.318). Our results indicate that inner Cd exposure may be a risk factor for depression, and physical activity can moderate this relationship to some degree.

Four most concerned heavy metal pollutants, arsenic, cadmium, lead, and mercury may share common mechanisms to induce metabolic syndrome (MetS). However, recent studies exploring the relationships between MetS and metal exposure presented inconsistent findings. We aimed to clarify the relationship between heavy metal exposure biomarkers and MetS using a meta-analysis and systematic review approach. Literature search was conducted in international and the Chinese national databases up to June 2020. Of selected studies, we extracted the relevant data and evaluated the quality of each study’s methodology. We then calculated the pooled effect sizes (ESs), standardized mean differences (SMDs), and their 95% confidence intervals (CIs) using a random-effect meta-analysis approach followed by stratification analyses for control of potential confounders. Involving 55,536 participants, the included 22 articles covered 52 observational studies reporting ESs and/or metal concentrations on specific metal and gender. Our results show that participants with MetS had significantly higher levels of heavy metal exposure [pooled ES = 1.16, 95% CI: 1.09, 1.23; n = 42, heterogeneity I² = 75.6%; and SMD = 0.22, 95% CI: 0.15, 0.29; n = 32, I² = 94.2%] than those without MetS. Pooled ESs in the subgroups stratified by arsenic, cadmium, lead, and mercury were 1.04 (95% CI: 0.97, 1.10; n = 8, I² = 61.0%), 1.10 (0.95, 1.27; 11, 45.0%), 1.21 (1.00, 1.48; 12, 82.9%), and 1.26 (1.06, 1.48; 11, 67.7%), respectively. Pooled ESs in the subgroups stratified by blood, urine, and the other specimen were 1.22 (95% CI: 1.08, 1.38; n = 26, I² = 75.8%), 1.06 (1.00, 1.13; 14, 58.1%), and 2.41 (1.30, 4.43; 2, 0.0%), respectively. In conclusion, heavy metal exposure was positively associated with MetS. Further studies are warranted to examine the effects of individual metals and their interaction on the relationship between MetS and heavy metals.

To date, micropollutants from anthropogenic sources cannot be completely removed from effluents of wastewater treatment plants and therefore enter freshwater systems, where they may impose adverse effects on aquatic organisms, for example, on fish. Advanced treatment such as ozonation aims to reduce micropollutants in wastewater effluents and, thus, to mitigate adverse effects on the environment. To investigate the impact and efficiency of ozonation, four different water types were tested: ozonated wastewater (before and after biological treatment), conventionally-treated wastewater, and water from a river (River Ruhr, Germany) upstream of the wastewater treatment plant effluent. Zebrafish (Danio rerio) embryos were used to study lethal and sublethal effects in a modified fish early life-stage test. Mortality occurred during exposure in the water samples from the wastewater treatment plant and the river in the first 24 h post-fertilization, ranging from 12% (conventional wastewater) to 40% (river water). Regarding sublethal endpoints, effects compared to the negative control resulted in significantly higher heart rates (ozonated wastewater), and significantly reduced swimming activity (highly significant in ozonated wastewater and ozone reactor water, significant in only the last time interval in river water). Moreover, the respiration rates were highly increased in both ozonated wastewater samples in comparison to the negative control. Significant differences between the ozonated wastewater samples occurred in the embryonic behavior and heart rates, emphasizing the importance of subsequent biological treatment of the ozonated wastewater. Only the conventionally-treated wastewater sample did not elicit negative responses in zebrafish, indicating that the discharge of conventional wastewater poses no greater risk to embryonic and larval zebrafish than water from the river Ruhr itself. The sublethal endpoints embryonic- and larval behavior, heart rates, and respiration were found to be the most sensitive endpoints in this fish early life-stage test and can add valuable information on the toxicity of environmental samples.

We conducted a meta-analysis to evaluate the association between prenatal cadmium (Cd) exposure and birth weight. PubMed, Embase, China National Knowledge Infrastructure (CNKI), and Wanfang databases were searched for studies published before March 2019. We used a model-based method, standardizing effect size from linear regression models to include a maximum number of studies during our quantitative evaluations. As a result, 11 articles from the general population, containing 10 birth cohorts and one cross-sectional study, were included. Our meta-analysis demonstrated that a 50% increase of maternal urine Cd (UCd) would be associated with a 6.15 g decrease in neonatal birth weight (β = −6.15 g, 95% CI: −10.81, −1.49) as well as a 50% increase of maternal blood Cd (BCd) would be associated with an 11.57 g decrease (β = −11.57 g; 95% CI: −18.85, −4.30). Stratified analysis of UCd data indicated that the results of female newborns were statistically significant (β = −8.92 g, 95% CI: −17.51, −0.34), as was the first trimester (β = −11.34 g, 95% CI: −19.54, −3.14). Furthermore, increased UCd levels were associated with a higher rate of low birth weight (LBW) risk (OR = 1.12, 95% CI: 1.03, 1.22). This meta-analysis demonstrated that elevated maternal Cd levels are associated with decreased birth weight and higher LBW risk.

Cadmium (Cd) was a developmental toxicant that induces fetal malformation and growth restriction in mice. However, epidemiological studies about the association of maternal serum Cd level with risk of preterm birth were limited. This study was to investigate whether maternal serum Cd level during pregnancy is associated with risk of preterm birth in a Chinese population. Total 3254 eligible mother-and-singleton-offspring pairs were recruited. Maternal serum Cd level was measured by GFAAS. Based on tertiles, maternal serum Cd concentration was classified as low (LCd, <0.65 μg/L), medium (MCd, 0.65–0.94 μg/L) and high (HCd, ≥0.95 μg/L). Odds ratio (OR) for preterm birth was estimated using multiple logistic regression models. Results showed the rate of preterm birth among LCd, M-Cd and HCd was 3.5%, 3.8%, and 9.4%, respectively. Subjects with HCd had a significantly higher risk for preterm birth (OR: 2.86; 95%CI: 1.95, 4.19; P < 0.001) than did those with LCd. Adjusted OR for preterm birth was 3.02 (95%CI: 2.02, 4.50; P < 0.001) among subjects with HCd compared to subjects with LCd. Taken together, the above results suggest that maternal serum Cd level during pregnancy is positively associated with risk of preterm birth.

Growing epidemiological evidence has shown that exposure to ambient air pollution contributes to poor sleep quality. However, whether variability in air pollution exposure affects sleep quality remains unclear. Based on a large sample in China, this study linked individual air pollutant exposure levels and temporal variability with subjective sleep quality. Town-level data on daily air pollution concentration for 30 days prior to the survey date were collected, and the monthly mean value, standard deviations, number of heavily polluted days, and trajectory for six common pollutants were calculated to measure air pollution exposure and its variations. Sleep quality was subjectively assessed using the Pittsburgh Sleep Quality Index (PSQI), and a PSQI score above 5 indicated overall poor sleep quality. Multilevel and negative control models were used. Both air pollution exposure and variability contributed to poor sleep quality. A one-point increase in the one-month mean concentration of particulate matter with aerodynamic diameters of ≤2.5 μm (PM₂.₅) and ≤10 μm (PM₁₀) led to 0.4% (95% confidence interval (CI): 1.002–1.006) and 0.3% (95% CI: 1.001–1.004) increases in the likelihoods of overall poor sleep quality (PSQI score >5), respectively; the odds ratios of a heavy pollution day with PM₂.₅ and PM₁₀ were 2.2% (95% CI: 1.012–1.032) and 2.2% (95% CI: 1.012–1.032), respectively. Although the mean concentrations of nitrogen dioxide, sulfur dioxide, and carbon monoxide met the national standard, they contributed to the likelihood of overall poor sleep quality (PSQI score >5). A trajectory of air pollution exposure with maximum variability was associated with a higher likelihood of overall poor sleep quality (PSQI score >5). Subjective measures of sleep latency, duration, and efficiency (derived from PSQI) were affected in most cases. Thus, sleep health improvements should account for air pollution exposure and its variations in China under relatively high air pollution levels.

The relation between pesticides exposure and metabolic syndrome (MetS) has not been clearly identified. Performing a systematic review and meta-analysis, PubMed, Cochrane Library, Embase, and ScienceDirect were searched for studies reporting the risk of MetS following pesticides exposure and their contaminants. We included 12 studies for a total of 6789 participants, in which 1981 (29.1%) had a MetS. Overall exposure to pesticides and their contaminants increased the risk of MetS by 30% (95CI 22%–37%). Overall organochlorine increased the risk of MetS by 23% (14–32%), as well as for most types of organochlorines: hexachlorocyclohexane increased the risk by 53% (28–78%), hexachlorobenzene by 40% (0.01–80%), dichlorodiphenyldichloroethylene by 22% (9–34%), dichlorodiphenyltrichloroethane by 28% (5–50%), oxychlordane by 24% (1–47%), and transnonchlor by 35% (19–52%). Sensitivity analyses confirmed that overall exposure to pesticides and their contaminants increased the risk by 46% (35–56%) using crude data or by 19% (10–29%) using fully-adjusted model. The risk for overall pesticides and types of pesticides was also significant with crude data but only for hexachlorocyclohexane (36% risk increase, 17–55%) and transnonchlor (25% risk increase, 3–48%) with fully-adjusted models. Metaregressions demonstrated that hexachlorocyclohexane increased the risk of MetS in comparison to most other pesticides. The risk increased for more recent periods (Coefficient = 0.28, 95CI 0.20 to 0.37, by year). We demonstrated an inverse relationship with body mass index and male gender. In conclusion, pesticides exposure is a major risk factor for MetS. Besides organochlorine exposure, data are lacking for other types of pesticides. The risk increased with time, reflecting a probable increase of the use of pesticides worldwide. The inverse relationship with body mass index may signify a stockage of pesticides and contaminants in fat tissue.